ArticleAntioxidants & redox signaling2014
S-nitrosoglutathione reductase deficiency-induced S-nitrosylation results in neuromuscular dysfunction.
Article in Antioxidants & redox signaling, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 47 citations in OpenAlex.
- The role of S-nitrosoglutathione reductase (GSNOR) in T cell-mediated immunopathology of experimental autoimmune encephalomyelitis (EAE).Neuroscience · 2025Article
- Nitrosative Stress in Astronaut Skeletal Muscle in Spaceflight.Antioxidants (Basel, Switzerland) · 2024Article
- A postpartum enriched environment rescues impaired cognition and oxidative markers in aged mice with gestational inflammation.Brain and behavior · 2022Article
- MitoTEMPOL modulates mitophagy and histopathology of Wistar rat liver after streptozotocin injection.Iranian journal of basic medical sciences · 2022Article
- The Protective Effect of Bergamot Polyphenolic Fraction (BPF) on Chemotherapy-Induced Neuropathic Pain.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Melatonin, Its Metabolites and Their Interference with Reactive Nitrogen Compounds.Molecules (Basel, Switzerland) · 2021Review
- Redox activation of ATM enhances GSNOR translation to sustain mitophagy and tolerance to oxidative stress.EMBO reports · 2021Article
- nNOS/GSNOR interaction contributes to skeletal muscle differentiation and homeostasis.Cell death & disease · 2019Article
- S-Nitrosoglutathione Reductase Is Essential for Protecting the Female Heart From Ischemia-Reperfusion Injury.Circulation research · 2018Article
- Pathophysiological Role of S-Nitrosylation and Transnitrosylation Depending on S-Nitrosoglutathione Levels Regulated by S-Nitrosoglutathione Reductase.Biomolecules & therapeutics · 2018Review
- Amelioration of spinal cord injury in rats by blocking peroxynitrite/calpain activity.BMC neuroscience · 2018Article
- S-nitrosoglutathione reductase (GSNOR) inhibitor as an immune modulator in experimental autoimmune encephalomyelitis.Free radical biology & medicine · 2018Article
- Article
- Article
- The mitochondrial metabolic reprogramming agent trimetazidine as an 'exercise mimetic' in cachectic C26-bearing mice.Journal of cachexia, sarcopenia and muscle · 2017Article
- Redox homeostasis and age-related deficits in neuromuscular integrity and function.Journal of cachexia, sarcopenia and muscle · 2017Review
- Remodeling adipose tissue through in silico modulation of fat storage for the prevention of type 2 diabetes.BMC systems biology · 2017Article
- The role of S-nitrosoglutathione reductase (GSNOR) in human disease and therapy.Critical reviews in biochemistry and molecular biology · 2017Review
- Hypoxia inducible factor-1 alpha stabilization for regenerative therapy in traumatic brain injury.Neural regeneration research · 2017Review
- GSNOR Deficiency Enhances In Situ Skeletal Muscle Strength, Fatigue Resistance, and RyR1 S-Nitrosylation Without Impacting Mitochondrial Content and Activity.Antioxidants & redox signaling · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsNitric oxide (NO) production is implicated in muscle contraction, growth and atrophy, and in the onset of neuropathy. However, many aspects of the mechanism of action of NO are not yet clarified, mainly regarding its role in muscle wasting. Notably, whether NO production-associated neuromuscular atrophy depends on tyrosine nitration or S-nitrosothiols (SNOs) formation is still a matter of debate. Here, we aim at assessing this issue by characterizing the neuromuscular phenotype of S-nitrosoglutathione reductase-null (GSNOR-KO) mice that maintain the capability to produce NO, but are unable to reduce SNOs.
resultsWe demonstrate that, without any sign of protein nitration, young GSNOR-KO mice show neuromuscular atrophy due to loss of muscle mass, reduced fiber size, and neuropathic behavior. In particular, GSNOR-KO mice show a significant decrease in nerve axon number, with the myelin sheath appearing disorganized and reduced, leading to a dramatic development of a neuropathic phenotype. Mitochondria appear fragmented and depolarized in GSNOR-KO myofibers and myotubes, conditions that are reverted by N-acetylcysteine treatment. Nevertheless, although atrogene transcription is induced, and bulk autophagy activated, no removal of damaged mitochondria is observed. These events, alongside basal increase of apoptotic markers, contribute to persistence of a neuropathic and myopathic state. INNOVATION: Our study provides the first evidence that GSNOR deficiency, which affects exclusively SNOs reduction without altering nitrotyrosine levels, results in a clinically relevant neuromuscular phenotype.
conclusionThese findings provide novel insights into the involvement of GSNOR and S-nitrosylation in neuromuscular atrophy and neuropathic pain that are associated with pathological states; for example, diabetes and cancer.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.